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作 者:郑峻松[1] 吴军[1] 彭代智[1] 肖光夏[1] 黎鳌[1] 李招权[2] 潘瑾[2]
机构地区:[1]第三军医大学西南医院烧伤研究所,重庆400038 [2]第三军医大学临床检验教研室
出 处:《中华实验外科杂志》2001年第6期551-553,共3页Chinese Journal of Experimental Surgery
基 金:国家自然科学基金资助项目 (3950 0 1 4 9)
摘 要:目的 探讨严重烧伤后小鼠脾脏T淋巴细胞功能受抑的胞内信号转导分子机制 ,并分析导致该改变的信号流“瓶颈”。方法 检测伤后早期 ( 2~ 168h)T细胞胞浆蛋白酪氨酸激酶(PTK)、蛋白激酶C(PKC)、肌醇磷脂特异性磷脂酶C (PI PLC)的活性改变和胞浆游离钙浓度变化 ,观察伤后T淋巴细胞增殖转化功能及白细胞介素 (IL) 2、IL 10分泌活性 ,分析各信号转导分子活性改变在导致伤后T细胞功能受抑中的作用。结果 胞浆PI PLC活性伤后 12h明显受抑( 13.89± 0 .12 ) μmol·mg-1·min-1,对照组 ( 16.5 2± 0 .48) μmol·mg-1·min-1,差异有显著性 (P <0 .0 5 ) ,伤后 168h恢复 ( 15 .2 6± 0 .12 ) μmol·mg-1·min-1;胞浆Ca2 +伤后 12h明显降低 (P <0 .0 5 ) ,显著降低持续到伤后 168h ;胞浆PTK活性升高 ,但仅伤后 12h升高显著 ( 34 .32± 4.2 2 )pmol·mg-1·min-1( P <0 .0 5 ) ;PKC活性呈现先升高 ( 2~ 12h)后降低 ( 2 4~ 168h)的双向改变。结论 PI PLC活性受抑 ,胞浆游离Ca2 +降低是伤后T细胞功能受抑的重要原因 ,胞浆PTK、PKC活性升高可能是对伤后T细胞胞外活化信号内流衰减的补偿。Objective To explore the mechanism of fun ction suppression of murine spleen T lymphocyte through intracellular signal tra nsduction,and to look for the crux which played restriction on the signal necle opetal transduction.Methods The changes of plasmic protein tyrosine kinase (P TK),protein kinase C (PKC),PI-PLC activivies and cytoplasmic calcium concentr ation were detected,the secretion of IL-2,IL-10 and the proliferating functi on of T cells at different postburn periods.Funthermore,the changes in the acti vities of various signal transduction molecules were analyzed with the considera tionof their relationship with the changes in T cell function activities.Results Cytoplasmic PI-PLC activity and were obviously decreased 12h after scalding (P<0.05) and returned to the normal 168 h after scalding as c ompared with those in the control group.Activity of plasmic PTK was significantl y increased 12h after scalding as compared with that in the control group (P <0.01).PKC activities were decreased after elevation.Conclusion The postburn suppression of PI-PLC activity a nd the decrease of cytoplasmic were the important factors for the suppression of IL-2 secretion,T cell dysfunction and the dual-directional ch ange in IL-10 production.
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